How nutrition is tested on Step 1

Vignettes give a risk setting (alcohol, malabsorption, diet, drug) and a sign; you name the vitamin or its biochemical role.

Fat-soluble vitaminDeficiencyExcess
A (retinol)Night blindness, dry eyes and Bitot spots, impaired immunityTeratogenic (isotretinoin), idiopathic intracranial hypertension, liver toxicity
DRickets (children), osteomalacia (adults), low calcium and phosphateHypercalcemia; also seen in granulomatous disease (sarcoidosis)
EHemolytic anemia, spinocerebellar and posterior column degenerationCan increase bleeding risk with warfarin
KBleeding with prolonged PT (factors II, VII, IX, X, proteins C and S)Rare

Newborns receive vitamin K at birth because their gut is sterile and breast milk is low in vitamin K.

B vitamins

Most B vitamins are enzyme cofactors; deficiency appears where those enzymes matter most.

B1 thiaminePyruvate and α-ketoglutarate dehydrogenase,transketolase; Wernicke, beriberiB2 riboflavinFAD, FMN; cheilosis, corneal vascularizationB3 niacinNAD, NADP; pellagra (3 Ds)B6 pyridoxineTransamination, heme and neurotransmitters;neuropathy, seizures, sideroblastic anemiaB9 folateOne-carbon transfer, DNA synthesis; megaloblasticanemia, neural tube defectsB12 cobalaminMethylmalonyl-CoA mutase, methionine synthase;anemia plus neurologic damage
B vitamins. Isoniazid causes B6 deficiency; give pyridoxine with it to prevent neuropathy.
B12 deficiencyMegaloblastic anemiaHomocysteine ↑ and methylmalonic acid ↑Neurologic: dorsal columns,corticospinal tractsPernicious anemia, ileal disease, vegandiet, metforminBody stores last yearsFolate deficiencyMegaloblastic anemiaHomocysteine ↑, methylmalonic acidnormalNo neurologic signsAlcohol, pregnancy, methotrexate,trimethoprim, phenytoinStores last monthsvs
B12 vs folate. Giving folate to a B12-deficient patient can correct the anemia while neurologic damage continues.

Vitamin C and minerals

Collagen synthesis and iron absorption link vitamin C to many findings.

  • Vitamin C: hydroxylates proline and lysine in collagen and keeps iron in the absorbable Fe²⁺ form. Scurvy causes gum disease, bruising, perifollicular hemorrhage, and corkscrew hairs.
  • Zinc deficiency: poor wound healing, loss of taste, alopecia, rash around the mouth and anus (acrodermatitis enteropathica).
  • Iron deficiency: microcytic anemia, low ferritin; in older adults, look for GI blood loss.

Protein-energy malnutrition

Both forms occur in children with inadequate diets; edema is the key difference.

Severe malnutritionKwashiorkorProtein ↓; edema, fattyliver, skin lesionsMarasmusCalories ↓; wasting, noedemaRefeeding riskHypophosphatemia, ↓K⁺, ↓Mg²⁺
Malnutrition. Kwashiorkor edema reflects low albumin and oncotic pressure; reintroduce nutrition gradually to avoid refeeding syndrome.

Worked example

Choose the right first treatment.

functions Worked example — confusion in the emergency department

A man with long-standing alcohol use disorder is confused, unsteady, and has nystagmus with lateral gaze palsy. His glucose is 52 mg/dL. What should be given first, and why?

  1. Confusion, ophthalmoplegia, and ataxia are the triad of Wernicke encephalopathy from thiamine deficiency.
  2. Thiamine is a cofactor for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase in glucose metabolism.
  3. Giving glucose without thiamine increases demand for the cofactor and can worsen brain injury.
  4. Give IV thiamine before or with the glucose.

Answer. IV thiamine before (or with) glucose to treat Wernicke encephalopathy.